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11(10), 438-448
Article DOI:10.21474/IJAR01/17725
DOI URL: http://dx.doi.org/10.21474/IJAR01/17725
RESEARCH ARTICLE
CLINICAL SUSPICION OF LEFT VENTRICULAR APICAL THROMBUS - WHAT TO DO?: A CASE
REPORT
It has been postulated that LVT provides a protection against LV rupture by extending a strong mechanical support
to the underlying myocardium, thus limiting the remodelling and LV scar formation (Figure 1).
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Figure 1:- Pathological specimen of LV apical thrombus. The thrombus is firmly attached to the apex and helps in
enhancing the underlying myocardial scar alongwith restoring the thickness of the myocardial wall.
The incidence of LVT complicating an AWMI has been significantly reduced to 5 % - 15 % [2-4], post early
revascularization and anticoagulation.
Currently, myriads of imaging modalities are at our disposal (Figure 2), to identify and illustrate the characteristics
of LVT: cardiac magnetic resonance (CMR), cardiac computed tomography (CCT), left ventriculography, strain
imaging utilising speckle tracking echocardiography, standard 2Dimensional transthoracic echocardiography (TTE)
and contrast echocardiography.
a) b)
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c) d)
e) f)
Figure 2:-
a) Cardiac Magnetic Resonance Imaging of LV apical thrombus.
b) Two reformatted gated CT images of the LV showing a filling defect (red arrow) in the apex, LA, left atrium, RA,
right atrium.
c) Left ventriculography in right anterior oblique view demonstrating a filling defect within the left ventricular apex
suggestive of an apical thrombus.
d) Strain imaging employing speckle tracking echocardiography. On the left panel (A) is “Bulls” eye mapping of
strain imaging in a patient without LV apical thrombus, and on the right panel (B) is a patient of LV apical
thrombus.
e) LV apical thrombus identified by standard 2D echocardiography.
f) Contrast echocardiography delineation of LV apical thrombus.
TTE remains the most versatile imaging technique to accomplish a diagnosis of LVT and has a sensitivity of 90-95
% and specificity of 85 - 95 % for detection of LVT [5, 6]. Asinger et al [7] enumerated the high risk
echocardiographic features for development of LVT (Table 1).
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CTI can be used for diagnosis and follow-up, as well as during interventional procedures. Its sophisticated
architecture based on linear pulser technology, is capable of managing various typologies of pulsing techniques in
order to optimize the beam forming management for a wide range of clinical applications.
Contrast-enhanced ultrasound has the advantages of the absence of ionizing radiation, widespread availability, even
at the bedside, and the possibility to characterize a lesion as soon as it is detected on conventional 2-Dimensional
echocardiography, commonly used as the first technique for exploration of the left ventricular opacification and
other areas [15].
In CTI second generation contrast agents are utilized for left ventricular opacification. However, in the current case
report we have employed CTI technology for left ventricular contrast echocardiography in the absence of
intravenous contrast agent, to recognize and substantiate the presence of AHCM. To our knowledge, this is a first
case report on CTI technology based contrast echocardiography for delineation of LVT.
Case Report
A 62 years old gentleman with a history of recent antero septal myocardial infarction (ASMI) diagnosed on resting
ECG was referred to us for a comprehensive color doppler echocardiography. He denied the presence of any major
cardiovascular risk factors. On clinical examination his pulse rate was 82/min, BP was 110/80 right upper limb in
seated position, SPO2 was 98% at room air and respiratory rate was 16/min. On cardiovascular examination, the
heart sounds were heard normally with the absence of clicks, murmurs or gallop sounds. Rest of the systemic
examination was normal. Pathological investigations were unremarkable. High sensitivity troponin-T and lipid
profile were within normal range. The resting ECG (Figure 3) identified the presence of pathological Q waves in
leads V₁ - V3 with T wave inversions in leads AVL and V1 - V5, consistent with sub-acute myocardial infarction.
Xray chest PA view (Figure 4) was normal with absence of cardiomegaly or pulmonary venous congestion.
Figure 3:- Resting ECG recognizes the presence of pathological Q waves in leads V1- V3 with T wave inversions in
AVL and V1- V5, consistent with subacute AWMI. Moreover, there is presence of Normal Sinus Rhythm with left
axis deviation.
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Figure 4:- X-ray Chest PA view appears to be normal. There is no cardiomegaly or pulmonary venous congestion.
a) b)
c) d)
Figure 5:- Standard 2Dimensional -,Transthoracic Echocardiography was performed in ( a), LX View, (b), SX
View,(c), 4CH View(c) and ( d)5CH View. There was presence of hypokinesia in anterior, mid septum, mid anterior
septum, apical and mid anterior wall (LAD Territory).
Presence of hypokinesia was recognised in anterior, mid septum, mid anterior septum apical and mid anterior wall,
suggestive of a ischemia in the left anterior descending artery territory. LV volumes and ejection fraction were
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estimated by utilizing biplane Simpson's method (Figure 6) and were observed to be normal. There was an absence
of any LV dilatation and the LVEF was normal (64%).
Figure 6:- Biplane Simpson’s method was adopted for calculation of LV volumes and LVEF. There was absence of
LV chamber dilatation with normal volumes and LV systolic function. LVEF was 64 %.
Pulse wave doppler (PWD) analysis (Figure 7) of mitral valve showed LV diastolic relaxation dysfunction (diastolic
dysfunction grade 1) and moreover tissue doppler imaging (TDI) estimated the E/E` ratio to be 7: 1 which is within
normal range.
a) b)
Figure 7:- (a), On the left panel pulse wave doppler at the tip of mitral valve showed LV diastolic relaxation
dysfunction (diastolic dysfunction grade 1), (b), On the right panel, tissue doppler Imaging of the LV estimated the
E/E’ ratio was 7:1 (within normal range).
Because of the presence of subacute ASMI, involving the LV apex, 4CH echocardiography in diastole and systole
was zealously attempted to rule out the presence of LVT.
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a) b)
Figure 8:- Transthoracic Echocardiography in 4CH View, (a), on the left panel in diastole and (b), on the right panel
in systole, reveals a hazy and unclear image of LV apical thrombus, highlighted by tracing the edges of the thrombus
with dotted line.
Nonetheless on contrast tuned imaging (CTI) based LV contrast echocardiography the LVT was distinctly
appreciated (Figure 9). The LVT was of moderate size (3.28 sq.cm), non pedunculated, mildly mobile and non-
calcified. (We want to clearly state that no intravenous contrast agent was used during this procedure).
a) b)
Figure 9:- Contrast Tuned Imaging Echocardiography distinctly portrayed the LV apical thrombus in (a), on the left
panel in diastole and (b), on the right panel in systole.
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a) b)
c) d)
e) f)
Figure 10:- 4Dimensional XStrain speckle tracking echocardiography-a) LV volumes, cardiac output, sphericity
index and ejection fraction were normal- LVEF 51.99 %, b) “Bulls” eye representation of polar mapping of LV
strain identified severely depressed values of LV strain - global LV strain, 2CH strain, LAX strain and 4CH strain
were -9.92 %, -8.88 %, -8.12 % and -12.75 % respectively, c) polar mapping of strain of all the LV segments
recognized marked depression of strain values in all the segments, particularly in the apical region , d- f) polar
mapping of LV strain in LAX, 2 CH and 4CH view conspicuously revealed LV strain values ranging from - 0.54 to -
1.94 % in the apical segments.
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Discussion:-
A LVT appears as an echo-dense mass distinct from the LV wall, but adjacent to an area of abnormal wall motion
[16]. Despite the widespread use of TTE, diagnostic performance is suboptimal with a sensitivity of only 33% and
specificity of 91% [11]. TTE can be technically challenging as a result of an indistinguishable myocardial-thrombus
interface, foreshortening of the LV apex or poor visualization of small protuberant thrombi or mural thrombi of any
size [6].
To visualize the LVT at the apex, the preferred imaging planes are the apical views, since the transducer is adjacent
to the LV apex. A thrombus has usually an echodensity similar to the myocardium while pannus appears more
hyperechoic [17].
AWMI in presence of apical dysfunction is a harbinger of escalated risk of LVT formation which may result in
systemic embolization [20, 21]. Even though 2Dimensional echocardiography is contemporarily the cornerstone for
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elucidating the LVT, nonetheless many a times it may not be adequate to recognise the hazy and unclear pictures of
LVT [10,11]. Thus it is advocated that extremely focussed LV apical echocardiographic examination to be
necessitated with a higher frequency transducer including a short focus for a highlighted near field resolution.
It is noteworthy that speckle tracking echocardiography has emerged as an established, objective and reproducible
method to determine the LV strain for early detection of multiple cardiac entities, regardless of the echocardiac
technique being employed [11 ,22, 23].
Conclusions:-
The diagnosis and management of LV thrombus after AMI is a clinical conundrum despite significant progress in
medical and device-based therapies. Early diagnosis of LV thrombus is critical to avoid thromboembolism, and the
choice of imaging modality and timing in relation to the incident myocardial infarction are important. Standard
echocardiography is often inconclusive or falsely negative regarding the detection of apical thrombus. There are
many studies and guidelines support the use of contrast to improve diagnostic accuracy, especially in patients with
suboptimal definition in routine echocardiography. Global longitudinal strain, particularly of the apical segments is
an independent risk factor for LVT formation in the apical region after AWMI. An early accurate thrombus
evaluation may prevent embolic complications, particularly cerebrovascular events. Assessment of ALS by
2Dimensional speckle tracking echocardiography is likely to become an a salient procedure in clinical practice. The
role of newer oral anticoagulants (NOACs) remains poorly defined, and vitamin K antagonists (VKA) remains the
mainstay of anticoagulation therapy until higher-quality evidence at least demonstrates noninferiority for the
prevention of thromboembolic events. Strategies that target Virchow's triad by mitigating myocardial injury and
preventing LV remodeling (stasis) and inflammation are likely to form the basis of the prevention and management
of LV thrombus well into the future.
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